The estimated lifetime prevalence of alcohol dependence (AD) or abuse (AA) among schizophrenics (SZ) is alarmingly high (34%) compared to that of the US population (13%). In addition, people with SZ who are comorbid for AA or AD exhibit treatment complications and poor outcomes. However, it is unknown why the prevalence of alcohol disorders is nearly three times higher in SZ than in the general population; nor is it known whether these dually diagnosed (DD) patients show additional and more profound pathophysiological deficits compared to non-AD schizophrenics. It is possible that alcohol dependence in SZ patients reflects a specific vulnerability to develop AD and that this comorbidity is, in fact, associated with more pronounced pathophysiology than seen in AD or SZ alone. Findings from family studies indicate that SZ and AA/AD may share common vulnerabilities or that dual independent vulnerabilities may underlie this form of psychiatric comorbidity. Very little is known about functional pathophysiological substrates of this comorbidity. Among the vulnerabilities that these comorbid SZ patients may have are psychohysiological deficits (e.g., P50, and auditory & visual P300) that have been independently associated with either SZ or AD. The purpose of this study is to determine the psychophysiological deficits associated with this dual diagnosis using well characterized electrophysiological measures that are sensitive and specific to each illness. We predict that abstinent SZ patients with a recent comorbid diagnosis of AD will not only manifest psychophysiological deficits widely associated with SZ, but will also show the psychophysiological deficits frequently associated with AD. Characterizing functional deficits across these measures in these groups will contribute to the identification of phenotypic subtypes, etiological mechanisms, and potential targets of treatment.